Coronary Heart Disease – Part III: Non-Modifiable Risk Factors

Suggested Citation: Garko, M.G. (2012, November). Coronary heart disease – Part III: Non-Modifiable Risk Factors. Health and Wellness Monthly. Retrieved (insert month, day, year), from www.letstalknutrition.com.

 

Coronary Heart Disease – Part III: Non-Modifiable Risk Factors

 

Michael Garko, Ph.D.

Host of Let’s Talk Nutrition

 

Introduction

 

“Sooner or later we all have to die of something.” This often heard statement reflects a fatalistic approach to health and wellness. Those who subscribe to it believe that trying to preserve and protect one’s health is fundamentally pointless because what will be, will be, that any health related event (e.g., a heart attack) in a person’s life is inevitable or otherwise predetermined.

 

While adopting a fatalistic approach to health and wellness may serve as a convenient way to rationalize away the concept of an increased risk (i.e., likelihood) for developing coronary heart disease (CHD), it is not without its consequences. For one thing, it fosters ignorance and inaction because it is predicated on the belief that learning about and avoiding modifiable risk behaviors (e.g., heavy alcohol and tobacco use, unhealthy diet, sedentary lifestyle, etc.), never mind non-modifiable ones (i.e., increasing age, gender, race-ethnicity and family history), will not make much of a difference in determining the course of a person’s health.

 

Furthermore, a fatalistic model of health and wellness renders the concept of making choices meaningless when it comes to a person’s health and wellness, and thereby, short circuits the principle of people taking personal responsibility for their health. It disempowers people and increases their likelihood of suffering from CHD or some other life threatening disease.

 

In the continuing effort to give health consumers the necessary information to take personal responsibility in preserving, protecting and promoting better health and reducing their chances of becoming debilitated by or dying from CHD, this November, 2012, issue of Health and Wellness Monthly examines the major non-modifiable risk factors for CHD.

Non-Modifiable Risk Factors For Coronary Heart Disease

 

Non-modifiable risk factors are fixed, unchangeable traits (e.g., age, gender and race-ethnicity). Increasing age and heredity are the two major categories of non-modifiable risk factors for CHD.

Increasing Age

CHD develops over the lifespan of an individual. As people age the more likely they are to develop CHD and suffer a fatal heart attack. After 40 years of age, the lifetime risk of developing CHD is 49% for men and 32% for women. More than four out of five or 81% of the people dying from CHD are 65 years of age or older[1] (see Roger et al., 2012).

Notwithstanding these statistics, reporting that increasing age is a risk factor tends to leave people feeling rather helplessness in combating CHD. The challenging unanswered question is, “How does increasing age become implicated in the development of CHD?”

As it turns out, research is being conducted on arterial and cardiac aging and why it is that cardiovascular disease (CVD)[2] is more likely in elderly persons (e.g., see Lakatta, 2003; Lakatta & Levey, 2003a, 2003b). Investigators are attempting to determine the ways in which the structure and function of the cardiovascular system changes over time and how those changes contribute to the risk of developing CHD. One proposed hypothesis is that age-related changes in the structure and function of the cardiovascular system become intertwined with disease-related processes which brought about by such risk factors as hypertension, inflammation, smoking and obesity, among others (see Lakatta & Levey, 2003a, 2003b).

The age-disease interaction hypothesis assumes that aging and disease formation are not necessarily one and the same process or at least they do not have to be. This holds important implications for how people think, feel and behave about their health, which will be discussed later.

Heredity

It is firmly established in the medical literature that heredity plays a significant role in the development of CHD. Heredity represents nature’s involvement in putting people at risk for CHD, while lifestyle is the nurture dimension for developing the disease. As a non-modifiable risk factor, heredity implicates gender, race-ethnicity and family history.

Gender

Prior to the 1990s, it was mistakenly believed that males suffered predominantly from CVD and CHD was a male disease. However, all of the various diseases of the heart and blood vessels constituting CVD make it the leading cause of death in the U.S. for both men and women (see Roger et al., 2012). Yet, only approximately 13% of women consider CVD to be the greatest risk to their health. No other disease, including cancer, claims as many women’s lives as does CVD. It is responsible for one death a minute among females, accounting for almost half-a-million female lives annually and women’s lives than are claimed by the next six leading causes of death combined (American Heart Association, 2006). Furthermore, the American Heart Association (2004) reported that one in three adult females is afflicted with some form of CVD and since 1984 the number of women’s deaths attributable to CVD has exceeded those for men.

With respect to CHD, it is the single leading cause of death of women in the United States. According to the American Heart Association (2004a), approximately three million women have a history of heart attack resulting from CHD. Thirty-eight percent of women suffering an initial heart attack will die from it within one year compared to 25% of men. Furthermore, “in part because women have heart attacks at older ages than men do, they’re more likely to die from them within a few weeks” (American Heart Association, 2004a, p. 6). Unfortunately, 64% of woman who die suddenly from CHD did not experience any previous symptoms. Menopause signals a time in women’s lives when their risk rises for CHD. The rate women contract CHD after menopause is 2-3 times those of women the same age before menopause (see American Heart Association, 2006). Hence, post-menopausal women need to be especially vigilant about CHD.

Although the statistics show women to be at risk for CVD, men have much about which they need to be concerned when it comes to diseases of the heart and blood vessels. One in four men suffers from some form of CVD. In its 44-year follow-up of participants and 20-year follow-up of their offspring,  the National Heart, Lung and Blood Institute’s (NHLBI) Framingham Heart Study (FHS) revealed that men experience their first major cardiovascular event (e.g., heart attack, stroke, congestive heart failure, angina, etc.) ten years earlier in life than women (see American Heart Association, 2004b). Even though this gap of ten years tends to narrow with advancing age, women’s risk for a heart attack after menopause fails to match the risk level for men (see American Heart Association, 2004a).

Just as with females, CHD is the single leading cause of death of males in America. Half of the men who die suddenly from CHD typically do not exhibit previous symptoms, death being their first and last symptom. Between 70%-89% of sudden cardiac deaths are associated with men, with the annual incidence being 3-4 times higher in men compared to women (Roger et al, 2012).

Within a period of six years after a heart attack, 18% of men will experience another heart attack, with 8% having a stroke, 7% experiencing sudden cardiac death and 22% becoming disabled with heart failure. Compared to women, men under the age of 75 have a higher proportion of cardiac events stemming from CHD than women. The average age for men who have their first heart attack from CHD is 65.8, while the average age for women is 70.4. The lifetime risk for men and women to develop CHD after age 40 is 49% and 32%, respectively. Lastly, the incidence of CHD for women lags 10 years behind men and 20 years behind men for more serious clinical events such as heart attack and sudden death (see American Heart Association, 2006; Roger et al., 2012).

In summary, CHD imposes serious health risks for both men and women. It is the single leading cause of death for both men and women. Thus, CHD is not a disease unique to men. Women are also clearly at risk for CHD and its consequences. Yet, men are even at greater risk when it comes to CHD and heart attacks. They tend to be at a greater risk than women for CHD and they have heart attacks earlier in life than women. Although the risk for women of having a heart attack increases subsequent to menopause, their risk never rises to level that of men.

Race-Ethnicity

Statistical studies indicate that racial-ethnic minorities are at risk for diseases of the heart and blood vessels, especially CHD. CVD is the leading cause of death among African-Americans. African-Americans, Mexican-Americans, American Indians, native Hawaiians and some Asian Americans have a higher risk for CHD than Caucasians. This is the case because non-whites (especially African-Americans) have more risk factors and higher rates of overweight and obesity, diabetes and high blood pressure, which are among the most serious risk factors for CHD (see American Heart Association, 2006, Roger et al, 2012).

Number of risk factors. The more risk factors a person has the greater the likelihood of developing CHD. African-American and Mexican-American women have more risk factors for CHD than Caucasian women who share a comparable socioeconomic status. The prevalence of having two or more risk factors for CHD among racial-ethnic minorities is highest among African-Americans, American Indians and Alaska Natives and lowest among Asians (see American Heart Association, 2006).

High blood pressure. HThe prevalence of HBP (hypertension) in African-Americans in America is considered to be among the highest world-wide. African-Americans ages 20-39 exhibit a higher prevalence of pre-hypertension than Caucasians and Mexican Americans. Compared to Caucasians, African-Americans develop full-blown HBP earlier in life and their average blood pressure is considerably higher. “As a result, compared with whites, blacks have a 1.3 times greater rate of nonfatal stoke, a 1.8 times greater rate of fatal stroke, a 1.5 times greater rate of heart disease death and a 4.2 time greater rate of end-stage kidney disease” (American Heart Association, 2006, p. 109). In comparison to Caucasian women, African-American women experience an 85% higher rate of ambulatory medical care visits for HBP.

Overweight  and Obesity. Although the obesity-overweight and obesity statistics in Caucasian, African-American and Mexican-American adult males are somewhat similar, African-American and Mexican-American adult females suffer from significantly higher rates of being overweight or obese than adult Caucasian females, putting these minority female groups at greater risk for CHD (see American Heart Association, 2006; Roger et al., 2012).

It is important to point out that a higher percentage of African-American and Mexican-American male and female children ages 6-11 and adolescents ages 12-19 suffer from being overweight than their Caucasian counterparts. This of course sets the stage for the children and adolescents from these minority groups to be at an even greater risk for becoming overweight or obese adults than their Caucasian counterparts.

Diabetes Mellitus. Based on a Medline search of 290 articles on diabetes, the U.S. Department of Health and Human Services Public Health Service through its Agency for Healthcare Research and Quality or AHRQ (2001) found that the burden of diabetes on minorities is greater than it is on Caucasians. Specifically, AHRQ (2001) reported that (1) all minorities, except for Alaska Native, are 2-6 times more likely to have Type 2 diabetes than Caucasians, (2) African Americans are from 1.4 – 2.2 times more likely to contract diabetes than Caucasians, (3) Hispanic-Americans have a higher prevalence of diabetes than non-Hispanics, (4) the prevalence of diabetes among American Indians is 2.8 times the overall rate, (5) primary groups within the Asian and Pacific Islander communities (i.e., Japanese Americans, Chinese Americans, Filipino Americans & Korean Americans) have higher prevalence rates for diabetes than Caucasians and (6) death rates related to diabetes for African-Americans, Hispanic Americans and American Indians were higher than those for Caucasians. In sum, given that it afflicts them in a sigificant way and given that it is major risk factor for the development CHD, there is little doubt that diabetes puts racial-ethnic minorities at risk for CHD.

Family History

Certain families seem to be more plagued with and predisposed to diseases of the heart and blood vessels than do other families. Medical researchers have devoted considerable attention to unraveling the ways in which family history becomes implicated with the different forms of CVD, including CHD. They have established that people are at a significantly increased risk for CVD when they have family members (especially first degree relatives & even second degree relatives) who have a history of (1) CVD (e.g., CHD, stroke, heart failure, angina pectoris, hypertension, etc.), (2) cardiac related events (e.g., myocardial infarction/heart attack & sudden death) and (3) cardiovascular risk factors (e.g., obesity, diabetes, adverse lipid/cholesterol profile, smoking, etc.) (see Bao et al., 1995; Barrett-Connor, E. et al., 1984; Blonde et al., 1981; Burke et al., 1991; Friedlander et al., 1998; Khaw & Barrett-Connor, 1986; Laskarzewski et al., 1981; Munger et al. 1988; O’Donnell, 2004; Sesso et al., 2001).

In an effort to understand the risk-raising connection of family history to CVD, medical researchers have attempted to identify those genes that predispose people to diseases of the heart and blood vessels (e.g., see Neufeld et al., 1983). For example, there are studies focusing on genetically transmitted cardiovascular diseases such as hypertrophic cardiomyopathy, Long-QT syndrome and Marfan syndrome that have a deleterious effect on the anatomic structure (heart size) and function (heart rate/muscle contraction) of the heart (e.g., see Ku et al., 2003; Maron et al., 1998; Singh et al., 1999).

There are also studies devoted to genes affecting the metabolic functioning of lipids and other bio-markers that have the potential to make people more susceptible bio-chemically and predisposed statistically to CHD and other types of CVD. For example, researchers have learned that certain gene mutations or variations can result in (1) high LDL cholesterol levels (2) low HDL cholesterol levels, (3) iron overload in the blood, (4) elevated homocysteine levels, (5) high Lp(a) levels, (6) increased triglyceride levels, (7) familial partial lipodystrophy (FPLD), (8) an increase in adipose tissue, among other genetically derived risks for CHD (e.g., see Life Extension Foundation, 2003).

Conclusion

It is clear from the scientific research presented above that increasing age and heredity have an impact on cardiovascular health. Since experts use such terms as “unchangeable,” “predetermined” and “uncontrollable” to describe them, the reader might wonder whether non-modifiable risk factors for CHD reinforce the fatalistic approach to health. Of course we all end up with a death certificate. However, our departure from this earth does not need to be premature. Nor does it need to be characterized by a protracted and debilitating illness of CHD brought on by a failure to take personal responsibility to prevent it (a hallmark of the fatalistic approach).

 

Heart-Healthy Choices

 

Some people are put at a potential health disadvantage by their increasing age or heredity or both. However, they do not have to live their lives with a feeling of impending doom created by the belief that they will die from CHD because of non-modifiable risk factors. Contrary to a fatalistic approach to health, we are not ill-fated when it comes to aging and heredity. Even with non-modifiable risk factors, we are not rendered helpless and without choices to prevent CHD.

 

One choice people can make is to become familiar with the non-modifiable factors associated with CHD. Having even a rudimentary understanding of non-modifiable risk factors can help people (1) determine if they may be at risk, (2) assess their level of risk, (3) teach them about and alert them to the early warning signs for CHD and (4) make them more vigilant and health conscious, all of which reduces the danger of suffering or dying from CHD.

 

Another choice people can make is to adopt a heart-healthy diet and lifestyle designed to modulate the effects of non-modifiable risk factors and prevent CHD. Generally speaking, a heart healthy diet and lifestyle would include day-to-day habits that prevent the atherosclerotic build-up of plaque in the coronary arteries, keep blood pressure from rising above normal levels and maintain the structure and function of the heart muscle.

 

A third option for people whose age or heredity (i.e., gender, race-ethnicity and family history) put them at risk for CHD is to keep the number of modifiable risk factors to a minimum (e.g., high blood pressure, diabetes, overweight-obesity, excessive tobacco and alcohol use, sedentary lifestyle, high LDL cholesterol and triglyceride levels, low HDL cholesterol levels, etc.). In addition to the scientific findings on the health consequences of having more rather than less risk factors for CHD, common sense dictates that the more non-modifiable and modifiable risk factors a person has the greater the likelihood for developing CHD and either becoming debilitated by or dying from it.

 

Non-modifiable Risk Factors As Modifiable

 

On the one hand, aging and heredity are non-modifiable in the sense that they possess programmed qualities. On the other hand, they are not immutable to the extent that people are left without any choices to moderate their impact on the development of CHD. Moreover, thinking about non-modifiable risk factors for CHD in less conventional terms opens the up the opportunity to make heart-healthy choices.

 

Aging. For example, rather than construing aging as a chronological phenomenon it is more useful to think about aging in functional/biological terms. That is, aging is not just about the passage of time. Rather, it is also about the bio-physical health status of a person at any given point in time. It is theoretically possible for an individual to be chronologically 50 but biologically 35 or chronologically 50 and biologically 65.

The point is that while chronological age (i.e., the passage of time) is non-modifiable, functional/biological age is modifiable. Diet/nutrition and lifestyle or otherwise what is put into the body and what is done to and with the body greatly influences the functional age of the body.

Heredity. Nutrition and lifestyle also influence the course of heredity. In this regard, a variation of an often cited principle is that genetics loads the gun, while diet and lifestyle pull the trigger. Even those who are gifted with a “healthy” set of genes can accelerate the process of aging and disease through poor diet and an unhealthy lifestyle. On the flipside of the genetic coin, individuals who may possess a set of genes making them more vulnerable to aging and disease can live a long and vibrant life through practicing nutritional and lifestyle principles that promote good health.

Preventing the potentially deleterious effects of non-modifiable risk factors for CHD is an achievable health goal. It all comes down to the nutritional and lifestyle choices that are made.

 

References

 

American Heart Association (2006). Heart disease and stroke statistics – 2006 Update. Dallas: A report from the American Heart Association Statistics Committee and Stroke Subcommittee, Texas: American Heart Association.

 

American Heart Association (2004a). Statistical fact sheet – populations: Women and cardiovascular diseases. Dallas, Texas: American Heart Association.

 

American Heart Association (2004a). Statistical fact sheet – populations: Men and cardiovascular diseases. Dallas, Texas: American Heart Association.

 

Bao, W., Srinivasan, S.S., Wattigney, W.A. & Berenson, G. (1995). The relation of parental cardiovascular disease to risk factors in children and young adults: The Bogalusa heart study. Circulation, 91, 365-371.

 

Barrett-Connor & Khaw, K.T., E. (1984). Family history of heart attack as independent predictor of death due to cardiovascular disease. Circulation, 69,  1065-1069.

 

Blonde, C.V. Webber, L.S., Foster, T.A., & Berenson, G.S. (1981). Parental history and cardiovascular disease risk factor variables in children. Preventive Medicine, 10, 25-37.

 

Burke, G.L., Savage, P.J., Sprafka, J.M., Selby, J.V., Jacobs, D.R., Perkins, L.L., Roseman, J.M., Hughes, G.H. & Fabsitz, R.R. (1991). Relation of risk factor levels in young adulthood to parental history of disease: The CARDIA study. Circulation, 84, 1176-1181.

 

Friedlander, Y., Siscovick, D.S., Weinmann, S., Austin, M.A., Psaty, B.M., Lemaitre, R.N., Arbogast, P., Raghumnathan, T.E. & Cobb, L.A. (1998). Family history as a risk factor for primary cardiac arrest. Circulation, 97, 155-160.

 

Khaw, K.T. & Barrett-Connor, E. (1986). Family history of heart attack: A modifiable risk factor? Circulation, 74  239-244.

 

Ku, L., Feiger, J. Taylor,M., Mestroni, L., and on behalf of the Familial Caridomyopathy Registry (2003). Circulation, 108, 118-121.

 

Lakatta, E.G. (2003). Arterial and cardiac aging: Major shareholders in cardiovascular disease enterprise: Part III: Cellular and molecular clues to heart and arterial aging. Circulation, 107, 490-497.

 

Lakatta, E.G. & Levy, D. (2003a). Arterial and cardiac aging: Major shareholders in cardiovascular disease enterprise: Part I: A “set up” for vascular disease, Circulation, 107, 139-146.

 

Lakatta, E.G. & Levy, D. (2003b). Arterial and cardiac aging: Major shareholders in cardiovascular disease enterprise: Part II: The aging heart in health: Links to heart disease. Circulation, 107, 346-354.

 

Laskarzewski, P., Morison, J.A., Horvitz, R. Khoury, P., Kelly K., Mellies, M. & Glueck, C.J. (1981). The relationship of parental istory of mycocardial infarction, hypertension, diabetes and stroke to coronary heart disease risk factors in their adult progeny. Journal of Epidemiology and Community Health, 113, 290-306.

 

Life Extension Foundation (2003). Cardiovascular disease: Comprehensive analysis. In M. Segala (Ed.), Disease prevention and treatment (pp. 423-528). Hollywood, FL: Life Extension Media.

 

Munger, R.G., Prieas, R.J. & Gomez,-Marin, O. (1988). Persistent elevation of blood pressure among children with a family history of hypertension: The Minneapolis children’s blood pressure study. Journal of Hypertension, 6,  647-653.

 

Neufeld, H.N. & Goldbourt, U. (1983). Coronary heart disease: Genetic aspects. Circulation, 67, 943-954.

 

Maron, B.J., Moller, J.H., Seidman, C.E., Vincent, M., Dietz, H.C., Moss, A.J., Towbin, J.A., Sondheimer, H.M., Pyeritz, R.E, McGee, G. & Epstein, A.E. (1998). Circulation, 98, 146001471.

 

O’Donnell, C.J. (2004). Family history, subclinical atherosclerosis, and coronary heart disease risk: Barriers and opportunities for the use of family history information in risk prediction and prevention. Circulation, 110, 2074-2076.

 

Roger, V., Go, A.S., Lloyd-Jones, D.M., Benjamin, E.J., Berry, J.D., Borden, W.B., Bravata, D.M., Dai, S., Ford, E.S., Fox, C.S., Fullerton, H.J., Gillespie, C., Hailpern, S.M., Heit, J.A., Howard, V.J., Kissela, jB.M., Kittner, S.J., Lackland, D.T.., Lichtman, J.H., Lisabeth, L.D., Makuc, D.M., Marcus, G.M., Marelli, A., Matchar, D.G., Mou, C.S., Mozaffarian, D., Mussolino, M.E., Nichol, G., Paynter, N.P., Soliman, E.Z., Sorlie, P.D., Sotoodehnia, N., Turan, T.N., Virani, S.S., Wong, N.D. Woo, D. & Turner, M.B. (2011). Heart disease and stroke statistics – 2012 Update: A report from the American Heart Association. Circulation. Retrieved January, 2012, from http://circ.ahajournals.org/content/early/2011/12/15/12/CIR.0b013e31823ac046.DC1.html

 

Sesso, H.D., Lee, I.M., Gaziano, J.M., Rexrode, K.M., Glynn, R.J., & Buring, J.E. (2001). Maternal and patenal history of myocardial infarction and risk of cardiovascular disease in men and women. Circulation, 104, 393-398.

 

Singh, J.P., Martin, G.L., O’Donnell, J., Hisako, T, Evans, J.C. & Levy, D. (1999). Circulation, 99, 2251-2254.

 

U.S. Department of Health and Human Services Public Health Service (2001). Fact sheet: Diabetes disparities among racial and ethnic minorities (AHRQ Publication No. 02-P007).

 

Suggested Citation: Garko, M.G. (2012, November). Coronary heart disease – Part III: Non-Modifiable  Risk Factors. Health and Wellness Monthly. Retrieved (insert month, day, year), from www.letstalknutrition.com.

 

 

 

 


[1] In addition to the age-related statistics for CHD, the statistics for other forms of CVD also show the role of increasing age as a risk factor for CVD (see Roger et al., 2012 for Heart Disease and Stroke Statistics – 2012 Update: A Report From the American Heart Association Statistics Committee and Stroke Statistics Subcommittee.

[2] CVD is used to mean diseases of the heart and blood vessels. CHD is a form of CVD. CHD includes heart attack and angina pectoris (see Roger et al., 2012.